Liu Yan, Cheng Yu, Chen Tianran, Wang Jun, He Jiajin, Yan Fuwu, Yan Lirong
Hubei Key Laboratory of Advanced Technology for Automotive Components, Wuhan University of Technology, Wuhan 430070, China; College of Automotive Engineering, Wuhan University of Technology, Wuhan 430070, China.
Hubei Key Laboratory of Advanced Technology for Automotive Components, Wuhan University of Technology, Wuhan 430070, China; College of Automotive Engineering, Wuhan University of Technology, Wuhan 430070, China; Department of Information, General Hospital of Central Theater Command, Wuhan 430070, China.
Brain Res. 2025 Jun 1;1856:149576. doi: 10.1016/j.brainres.2025.149576. Epub 2025 Mar 18.
This study investigates the impact of basal ganglia network asymmetry on motor function in Parkinson's Disease (PD). Using resting-state functional magnetic resonance imaging (rs-fMRI), functional connectivity and network asymmetry were analyzed in 15 non-demented PD patients and 15 healthy controls. Sixteen basal ganglia substructures, including the caudate, putamen, and globus pallidus, were selected for a unified analysis of variance framework to evaluate inter-hemispheric connectivity differences. After spatial preprocessing, regions of interest were defined, and time-series data were extracted for functional connectivity and network asymmetry analysis. The results revealed significant alterations in the functional connectivity of the caudate, putamen, and nucleus accumbens (NAc) in PD patients. Notably, the absence of intra-network asymmetry in the left NAc and bilateral amygdala correlated with motor dysfunction, likely due to overactivity of the inhibitory indirect pathway. Furthermore, pronounced asymmetry in the left putamen and right frontal gyrus suggested a compensatory neural mechanism supporting motor performance. These findings highlight the critical role of basal ganglia network asymmetry in the pathophysiology of PD. The identified asymmetry characteristics may serve as potential biomarkers for early diagnosis and disease progression monitoring, offering new directions for targeted therapeutic interventions.
本研究调查了基底神经节网络不对称性对帕金森病（PD）运动功能的影响。使用静息态功能磁共振成像（rs-fMRI），对15名非痴呆PD患者和15名健康对照者的功能连接性和网络不对称性进行了分析。选择包括尾状核、壳核和苍白球在内的16个基底神经节亚结构，用于统一方差分析框架，以评估半球间连接性差异。在进行空间预处理后，定义感兴趣区域，并提取时间序列数据进行功能连接性和网络不对称性分析。结果显示，PD患者的尾状核、壳核和伏隔核（NAc）的功能连接性有显著改变。值得注意的是，左侧NAc和双侧杏仁核内网络不对称性的缺失与运动功能障碍相关，这可能是由于抑制性间接通路的过度活跃所致。此外，左侧壳核和右侧额回的明显不对称表明存在支持运动表现的代偿性神经机制。这些发现突出了基底神经节网络不对称性在PD病理生理学中的关键作用。所确定的不对称特征可能作为早期诊断和疾病进展监测的潜在生物标志物，为靶向治疗干预提供新的方向。
